The following will be studied: (1) the role of uvrD plus in the control of the excision repair patch size produced by polA plus; (2) the genetic control and nature of high UV dose mutagenesis; (3) is the repair performed during liquid holding recovery mutagenic; (4) quantify the role of polA ion in low UV dose postreplication repair that is inhibitable by complex growth medium. The following will be completed: (1) the role of polB in long patch excision repair; (2) the general role of uvrD in excision repair; (3) the in vitro X-ray sensitivity of fibroblasts from patients showing an unusual skin sensitivity to radiation therapy; (4) the role of recB and uvrD in low dose mutagenesis.